A longitudinal comparison of the cardiovascular responses of monozygotic and dizygotic twins is proposed to test the following hypotheses: (1) The hemodynamic determinants of blood pressure (heart size, cardiac output and systemic vascular resistance) and left ventricular mass are more strongly influenced by genetic factors than blood pressure itself. (2) Homologous hemodynamic measurements in young males and females are controlled by the same genes. (3) The cardiovascular responses to isometric and dynamic exercise are controlled by the same genes as those which influence resting values. (4) The same genes control the cardiovascular responses of twins before and after the onset of puberty. (5) The blood pressures of parents are more closely related to the hemodynamic determinants of their children's blood pressure than they are to the blood pressures measurements themselves. We will recruit a sample of 330 preadolescent twin pairs stratified by sex and zygosity from an established population based twin registry, and collect resting noninvasive hemodynamic measures of cardiac output and left ventricular mass using the echocardiogram, as well as measurement of blood pressure. The zygosity will be accessed by questionnaire and confirmed by dermatoglyphic analysis and blood group tests. The anthropometric and hemodynamic measurements in the parents will be compared to those measurements in the twin children. The children will also have an isometric stress test with measurement of echocardiographic cardiac output blood pressure and heart rate. A submaximal dynamic exercise test will also be performed while blood pressure and heart rate are monitored. Three cohorts of 11-year-old twins will initially be evaluated in a cross-sectional study and then followed longitudinally for up to 3 years. The availability of repeated measures of blood pressure and their determinants hemodynamic on twins will permit a unique analysis of the effects of genetic environmental factors and the process of developmental change. The longitudinal study has the potential for elucidating the cause of cardiovascular variation during maturation. Analysis of the resulting data will permit tests of the proposed hypotheses and a more sophisticated treatment of the tracking phenomena than has heretofore been possible.